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Article
January 1960

Pathogenetic Factors in Experimental Galactose CataractPart III

Author Affiliations

Rochester, N.Y.
From the Department of Surgery, Division of Ophthalmology, of the University of Rochester School of Medicine and Dentistry.

AMA Arch Ophthalmol. 1960;63(1):136-139. doi:10.1001/archopht.1960.00950020138021
Abstract

The cataractogenic action of galactose is apparently due to a marked inhibition in the direct oxidative pathway of glucose-6-phosphate metabolism.1 The accumulation of galactose-1-phosphate in the lenses of animals maintained on a galactose diet2 acts as or gives rise to a specific inhibition of the enzyme glucose-6-phosphate dehydrogenase (G-6-P dehydrogenase).3 Since this enzyme is responsible for the first step in the direct oxidation of glucose-6-phosphate (G-6-P) to 6-phosphogluconate (6-P-G), an inhibition at this locus results in a marked depression of the hexose monophosphate shunt. In the experimental rat lens this inhibition occurs after the animal has been fed a 70% galactose diet for two and one-half to three days.1,3 Three to four days later, the synthesis of soluble lens proteins apparently ceases1,4; lens vacuoles first become manifest after 9-10 days on this diet, and a dense cataract develops in 12-18 days.

Since a sufficient supply

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